Glucocorticoids regulate a remarkable variety of essential functions, including development, immunomodulation, maintenance of circadian rhythm and the response to stress. Glucocorticoids acutely increase energy availability; this is accomplished not only by mobilizing energy stores but also by diverting energy away from anabolic processes in tissues such as skeletal muscle and bone. While this metabolic shift is advantageous in the short term, prolonged glucocorticoid exposure frequently results in central obesity, insulin resistance, hyperglycaemia, dyslipidaemia, muscle wasting and osteoporosis. Understanding how glucocorticoids affect nutrient partitioning is, therefore, critical for preventing the side effects of glucocorticoid treatment. Independently of circulating glucocorticoids, intracellular glucocorticoid activity is regulated by the 11β-hydroxysteroid dehydrogenases 1 and 2 (HSD11B1 and 2), which activate and inactivate glucocorticoids, respectively. Excessive HSD11B1 activity and amplification of local glucocorticoid activity in tissues such as adipose tissue and bone may contribute to visceral obesity, insulin resistance and ageing-related bone loss in humans. Several recent findings in animals have considerably expanded our understanding of how glucocorticoids exert their dysmetabolic effects. In mice, disrupting glucocorticoid signalling in either adipose tissue or bone produces marked effects on energy homeostasis. Glucocorticoids have also been shown to influence brown adipose tissue thermogenesis (acute activation, chronic suppression), in both rodents and humans. Lastly, recent studies in mice have demonstrated that many dysmetabolic effects of glucocorticoids are sexually dimorphic, although corresponding results in humans are lacking. Together, these studies have illuminated mechanisms by which glucocorticoids exert their metabolic effects and have guided us towards more targeted future treatments for metabolic diseases.

糖皮质激素调节多种重要功能，包括发育、免疫调节、昼夜节律的维持和对压力的反应。糖皮质激素急剧增加能量供应；这不仅可以通过调动能量储存来实现，还可以通过将能量从骨骼肌和骨骼等组织中的合成代谢过程中转移出来。虽然这种代谢转变在短期内是有利的，但长期接触糖皮质激素经常导致向心性肥胖、胰岛素抵抗、高血糖、血脂异常、肌肉萎缩和骨质疏松症。因此，了解糖皮质激素如何影响营养分配对于预防糖皮质激素治疗的副作用至关重要。独立于循环糖皮质激素，细胞内糖皮质激素活性受 11β-羟基类固醇脱氢酶 1 和 2（HSD11B1 和 2）调节，它们分别激活和灭活糖皮质激素。脂肪组织和骨骼等组织中过度的 HSD11B1 活性和局部糖皮质激素活性的增强可能导致人类内脏肥胖、胰岛素抵抗和与衰老相关的骨质流失。最近在动物身上的几项发现大大扩展了我们对糖皮质激素如何发挥其代谢障碍作用的理解。在小鼠中，破坏脂肪组织或骨骼中的糖皮质激素信号对能量稳态产生显着影响。糖皮质激素也已被证明会影响啮齿动物和人类的棕色脂肪组织产热（急性激活、慢性抑制）。最后，最近对小鼠的研究表明，糖皮质激素的许多代谢障碍作用是性别二态的，尽管在人类中缺乏相应的结果。总之，这些研究阐明了糖皮质激素发挥其代谢作用的机制，并指导我们对代谢疾病进行更有针对性的未来治疗。